Nicotine receptors were visualized in rhesus monkey brain with autoradiographic procedures. Binding was heaviest in various thalamic nuclei. Relatively heavy labeling was also found in the geniculate nuclei and substantia nigra. In cortex, nicotine receptors were restricted to layer II. In rat nicotine receptors were found on both the terminals and cell bodies of dopamine neurons. In the interpeduncular nucleus nicotine receptors were localized both presynaptically and postsynaptically to Ach neurons. Lesion studies revealed that dopamine perikarya do not contain opiate receptors. Opiate receptors in the substantia nigra appear to be located on terminals of striato-nigral afferents. 3H-cyclo-foxy (an opiate ligand that can also be fluorinated) was shown to produce identical binding patterns in rat brain following in vivo or in vitro application. This novel ligand has potential use in PET applications. In hamsters, the sexually dimorphic nucleus in the male showed denser opiate receptor binding than in female. Pattern differences also appeared in opiate receptor binding in the hypothalamus between sexes. In vivo autoradiographic procedures revealed differences in 3H-diprenorphine binding densities between control males and mated males in various hypothalamic nuclei, suggesting enhanced release of endogenous opiates during mating. Electrical stimulation of the arcuate nucleus also produced decreased binding of 3H-diprenorphine in terminal areas of the beta-endorphin system suggesting release of beta-endorphin. Such stimulation was also accompanied by a naloxone reversible analgesia. Morphine raised aversive brain-stimulation thresholds in the mesencephalic reticular formation while neurotensin lowered thresholds. Autoradiographic analyses revealed exceptionally heavy binding of salmon calcitonin in the nucleus accumbens. Calcitonin receptors were found to be postsynaptic to dopamine (DA) terminals in the n. accumbens but located on DA cell bodies in the substantia nigra. Injections of salmon calcitonin into the n. accumbens produced profound depression of locomotor behavior. Phencyclidine was found to enhance locomotor output through the n. accumbens by a DA independent mechanism.